Endothelial Dysfunction in HIV-Infected Sickle Cell Disease Patients: A Review

Endothelial dysfunction is a significant complication in patients with both sickle cell disease (SCD) and human immunodeficiency virus (HIV) infection, contributing to increased morbidity and mortality. In SCD, chronic hemolysis leads to elevated levels of free hemoglobin and reactive oxygen species, resulting in decreased nitric oxide (NO) availability and impaired endothelial function. Concurrently, HIV infection is characterized by persistent immune activation and inflammation, further exacerbating endothelial injury. The interplay between these two conditions creates a synergistic effect that heightens the risk of thrombotic events, cardiovascular disease, and organ damage. This review aims to elucidate the molecular mechanisms underlying endothelial dysfunction in SCD-HIV co-infected patients, focusing on the roles of oxidative stress, inflammatory cytokines, and the upregulation of endothelial adhesion molecules. We also examine the contributions of dysregulated coagulation pathways to the vascular complications observed in this population. Understanding these mechanisms is crucial for developing effective therapeutic strategies to mitigate endothelial dysfunction and improve patient outcomes.